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ACSS3蛋白质大分子通过Wnt/β-catenin信号通路调节 keloid 中的糖解:生物信息学,机器学习和实验验证

Pingping Huo¹, Sujie Wang², Zhouna Li³

¹Keloid Research Center, Department of Dermatology, Yanbian University Hospital, 1327 Ju Zi Street, Yanji 133000, China; Yanbian University Medical College, 977 Gongyuan Street, Yanji 133002, China.

Cellular signalling

|August 9, 2025

概括

状纤维细胞表现出代谢重编程. 这项研究确定了乙-CoA合成酶短链家族成员3 (ACSS3) 作为通过Wnt/β-Catenin通路调节 keloid 纤维细胞活性和有氧糖解的关键调节者.

科学领域:

皮肤病学皮肤病学
分子生物学分子生物学
生物信息学是一种生物信息学.

背景情况:

质体是异常的伤口愈合反应,其特征是过度纤维细胞生长和代谢变化.
驱动化纤维细胞 (KF) 代谢重编程的精确机制尚未完全理解.

研究的目的:

调查乙-A合成酶短链家族成员3 (ACSS3) 和Wnt/β-catenin通路在 keloid 病原发生中的作用.
确定ACSS3作为潜在的治疗化物治疗的治疗标.

主要方法:

生物信息分析以确定关键分子参与者.
在KFs中操纵ACSS3表达的lentiviral转染.
糖溶性流体分析和酶水平评估.
单细胞RNA测序. 一个单细胞RNA测序.
分子对接和动力学模拟.

主要成果:

发现ACSS3在胆固醇中被降低调节,其过度表达抑制了KF活性并使糖解正常化.
ACSS3敲击增加了KF活性和糖溶性流量,ICG-001.1.反转了这些影响.
纤维细胞被确定为 keloid 纤维化中的主要细胞类型.
建立了ACSS3的监管网络,并确定了针对ACSS3的潜在候选药物.

结论:

通过Wnt/β-Catenin通路,ACSS3在调节 keloid 纤维细胞活性和有氧糖解方面发挥着至关重要的作用.
ACSS3代表了一种有前途的治疗点,用于控制胆固醇形成和进展.

关键词:

在ACSS3中,我们使用了ACSS3.葡萄糖溶解是什么? 葡萄糖溶解凯洛伊德 (Keloid) 是一种类型的细胞.

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